https://www.selleckchem.com/pr....oducts/ly3200882.htm
Moreover, INSR inactivated JAK2/STAT3 pathway in OA chondrocytes. Dual luciferase report and CHIP assay results confirmed that INSR was transcriptionally regulated by KLF4. As shown in MS-PCR results, INSR expression was mediated by DNA methylation in OA. Our findings suggested that INSR, as a key regulator for OA, was regulated by transcription factor KLF4 and DNA methylation, thereby mediating the activation of JAK2/STAT3 signaling, which was considered as an underlying therapeutic target for OA. Our findings suggested that INSR, as
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